The capacity of macrophages (MΦ) to oxidize LDL, produce ceroid (CR), and transform into foam cells (FC) is enhanced following erythrophagocytosis. During the process of FC formation, part of hemoglobin-derived iron forms a complex with CR. CR is cytotoxic; and over time, it can lead to FC apoptosis. Release of CR from apoptotic FC into the surrounding tissue may cause dysfunction and apoptosis of newly invading MΦ. Given that lipid and iron deposits within hemorrhagic MI (hMI) typically colocalize in the infarct periphery, we hypothesized that CR from apoptotic FC promotes perpetual MΦ ingress and localized edema formation in hMI.
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